Intracerebral haemorrhage (ICH) accounts for about 10–15% of all strokes and is associated with high mortality and morbidity. Despite extensive research, there is no successful Phase III clinical trial for ICH. Over the past six years, there has been a significant increase in pre-clinical and clinical studies on ICH, leading to a better understanding of the mechanisms of brain injury and potential therapeutic targets. This review summarizes the current knowledge on ICH, including its mechanisms, therapeutic approaches, and clinical trials. ICH is a stroke subtype with high mortality (around 40% at one month) and often results in major neurological impairments. It is the most common cause of spontaneous ICH, with other causes including amyloid angiopathy, brain tumors, aneurysms, and cerebral cavernous malformations. Anticoagulant-related ICH is becoming more frequent, accounting for nearly 20% of ICH cases in the USA. ICH can occur in various locations, including the putamen, caudate, thalamus, lobar, cerebellar, and pontine regions. Asymptomatic microbleeds are also common and may indicate underlying vascular pathology. The natural history of ICH involves initial physical disruption of the brain, leading to increased intracranial pressure and potential brain herniation. Haematoma expansion within the first day after ICH can worsen outcomes. Brain oedema develops rapidly after ICH and peaks in the second week. The haematoma gradually resolves over weeks, leaving a cavity with brain tissue destruction. Animal models of ICH include direct blood or collagenase injection into the brain. These models have been used to study the mechanisms of ICH-induced brain injury. Pre-clinical studies have focused on the role of thrombin, inflammation, and other factors in ICH-induced injury. Thrombin plays a central role in haemostasis but can also contribute to ICH-induced injury through inflammatory responses and cell death pathways. Inflammation is a significant factor in ICH-induced injury, with microglia activation and neutrophil infiltration playing key roles. Complement activation and haemoglobin/iron release from the haematoma also contribute to brain injury. Free radicals and iron are involved in tissue damage, and agents such as deferoxamine and inhibitors of haem oxygenase have shown promise in reducing ICH-induced injury. Therapeutic approaches include clot removal, blood pressure management, and agents targeting inflammation and free radicals. However, most clinical trials have not shown significant benefits. Pre-clinical studies have identified several potential therapeutic targets, but translating these into successful clinical trials remains a challenge. The review highlights the need for further research to develop effective treatments for ICH.Intracerebral haemorrhage (ICH) accounts for about 10–15% of all strokes and is associated with high mortality and morbidity. Despite extensive research, there is no successful Phase III clinical trial for ICH. Over the past six years, there has been a significant increase in pre-clinical and clinical studies on ICH, leading to a better understanding of the mechanisms of brain injury and potential therapeutic targets. This review summarizes the current knowledge on ICH, including its mechanisms, therapeutic approaches, and clinical trials. ICH is a stroke subtype with high mortality (around 40% at one month) and often results in major neurological impairments. It is the most common cause of spontaneous ICH, with other causes including amyloid angiopathy, brain tumors, aneurysms, and cerebral cavernous malformations. Anticoagulant-related ICH is becoming more frequent, accounting for nearly 20% of ICH cases in the USA. ICH can occur in various locations, including the putamen, caudate, thalamus, lobar, cerebellar, and pontine regions. Asymptomatic microbleeds are also common and may indicate underlying vascular pathology. The natural history of ICH involves initial physical disruption of the brain, leading to increased intracranial pressure and potential brain herniation. Haematoma expansion within the first day after ICH can worsen outcomes. Brain oedema develops rapidly after ICH and peaks in the second week. The haematoma gradually resolves over weeks, leaving a cavity with brain tissue destruction. Animal models of ICH include direct blood or collagenase injection into the brain. These models have been used to study the mechanisms of ICH-induced brain injury. Pre-clinical studies have focused on the role of thrombin, inflammation, and other factors in ICH-induced injury. Thrombin plays a central role in haemostasis but can also contribute to ICH-induced injury through inflammatory responses and cell death pathways. Inflammation is a significant factor in ICH-induced injury, with microglia activation and neutrophil infiltration playing key roles. Complement activation and haemoglobin/iron release from the haematoma also contribute to brain injury. Free radicals and iron are involved in tissue damage, and agents such as deferoxamine and inhibitors of haem oxygenase have shown promise in reducing ICH-induced injury. Therapeutic approaches include clot removal, blood pressure management, and agents targeting inflammation and free radicals. However, most clinical trials have not shown significant benefits. Pre-clinical studies have identified several potential therapeutic targets, but translating these into successful clinical trials remains a challenge. The review highlights the need for further research to develop effective treatments for ICH.